The kidneys function to rid the body of metabolic and ingested waste products and to maintain the volume and composition of bodily fluids. The maintenance of a constant extracellular fluid (ECF) composition by the kidneys is accomplished by various neural, hormonal, and intrinsic homeostatic mechanisms that control the rate at which blood is filtered by the glomerulis, referred to as the glomerular filtration rate (GFR), and the extent to which sodium and water are reabsorbed from the filtrate into the peritubular capillary blood.
The kidneys normally act to maintain both arterial blood pressure and ECF volume within desired normal ranges. However, in certain pathological situations, homeostatic mechanisms do not respond in an appropriate manner. One situation in which the homeostatic mechanisms of the kidneys may not respond in an optimal manner is during heart failure. Heart failure refers to a clinical syndrome in which an abnormality of cardiac function causes a below normal or normal ejection fraction and pathophysiological ventricular hypertrophy which often results in reduction in cardiac output. Such a reduction in cardiac output can fall below a level adequate to meet the metabolic demand of peripheral tissues. Reduced cardiac output has a depressing effect on renal function due to decreased renal perfusion, which causes a reduction in salt and water excretion by the pressure natriuresis mechanism. The renin-angiotensin-aldosterone system also promotes water and plasma volume retention to compensate for the reduced cardiac output. The increased sympathetic activity in response to low blood pressure and/or cardiac output may also depress renal function still further.
The increased fluid retention by the kidneys results in an increased blood volume and further increased venous return to the heart, thus increasing the heart's preload. This process is acutely beneficial in supplementing and maintaining adequate cardiac output, however this process can result in deleterious changes long-term. Increased fluid retention causes the progressive peripheral and pulmonary edema that characterizes overt congestive heart failure. As part of downward spiral, diastolic filling pressure becomes further elevated which causes the heart to become so dilated and edematous that its pumping function deteriorates even more.
One approach to treating heart failure is to modulate renal function through pharmacological means. For example, diuretic drugs can be used to decrease the tubular reabsorption of salt and water, leading to reduced fluid retention (increased fluid excretion). However, such pharmacological agents are not always effective and they may cause significant side effects. In addition, patient compliance with pharmacological regimens is a serious problem.
For at least these reasons, a need exists for devices and methods for modulating renal function.